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The objective of the presented work was a quantitative analysis of causes of ruptures of laparotomic wounds with emphasis on risk factors, and thus a contribution to the prevention of the mentioned complication. Complete rupture of laparotomic wounds such as eventration are encountered most frequently in interaction of high intraabdominal pressure and weakness of the suture. Continuous loop stitch is the optimal closure of laparotomy. The authors evaluated in a retrospective study a group of 21 patients with eventration and found a coincidence of causes increasing the risk of rupture of the laparotomic wound. From the quantitative aspect serious causal factors include the length and urgency of primary surgery, infection of the wound, a combination of pathogenetic factors such as malignancy, diabetes, anaemia, obesity and hypoproteinaemia. The interaction of different causes increases the risk of wound rupture in all four stages of healing of the surgical wound.
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PMID:[Causes of rupture in laparotomy incisions]. 1051 Jun 29

Knee flexion contractures in spina bifida patients are seen in all levels of paralysis. The majority is encountered in children with thoracolumbar lesions. Positional deformation, spinal reflex activity, fractures around the knee joint and a weak quadriceps are the main causes of the flexion deformity of the knee. One hundred and forty-five knee flexion contractures in 80 children have been treated between 1980 and 1995; 15 with unilateral contracture, 65 with bilateral involvement. The age at the time of correction in 38 patients with thoracolumbar lesions was between 24 months and 11 years (average, 7.7 years). In 42 patients with sacral or lumbosacral lesions, the age at the time of correction was between 10 and 19 years (average, 16.3 years). Associated surgery was mainly carried out on hip flexors, adductors and triceps surae. Complete posterior release was practiced in thoracolumbar lesions including posterior capsulotomy and release of the posterior cruciate ligament. In lumbosacral lesions, the lengthened tendons are sutured to prevent flexor weakness in the postoperative course. Vascular and neurologic structures are spared. Postoperative serial casts are helpful to achieve full extension without vascular or skin troubles. The long-term results were very good in 59 patients with 106 knees, good in 16 patients with 29 knees, and unsatisfactory in 5 patients with 10 knees. Slow deterioration years after surgery can be anticipated. The main causes are lack of personal initiative to stand and to walk, and obesity.
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PMID:Follow-up study after treatment of knee flexion contractures in spina bifida patients. 1090 1

Knee OA in the older adult is often the result of multiple factors, some of which are intrinsic to the joint tissues and related to aging and others, such as obesity, which are extrinsic and influence the rate of development and severity of the disease. Obesity and quadricep weakness are factors that may be modifiable. The focus in managing patients with knee OA should not only be centered on the improvement of pain but also improvement in function. A combination of simple analgesics and nonpharmacologic measures, including exercises to strengthen the knee extensors, should be employed. Patients also can benefit from aerobic exercises, such as a walking or swimming program and strategies for joint protection. When medications are needed, the least toxic drugs possible should be used given the increased susceptibility of older adults to unwanted side effects.
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PMID:Aging and the etiopathogenesis and treatment of osteoarthritis. 1098 12

Osteoarthritis is the most common form of arthritis, affecting millions of people in the United States. It is a complex disease whose etiology bridges biomechanics and biochemistry. Evidence is growing for the role of systemic factors (such as genetics, dietary intake, estrogen use, and bone density) and of local biomechanical factors (such as muscle weakness, obesity, and joint laxity). These risk factors are particularly important in weight-bearing joints, and modifying them may present opportunities for prevention of osteoarthritis-related pain and disability. Major advances in management to reduce pain and disability are yielding a panoply of available treatments ranging from nutriceuticals to chondrocyte transplantation, new oral anti-inflammatory medications, and health education. This article is part 1 of a two-part summary of a National Institutes of Health conference. The conference brought together experts on osteoarthritis from diverse backgrounds and provided a multidisciplinary and comprehensive summary of recent advances in the prevention of osteoarthritis onset, progression, and disability. Part 1 focuses on a new understanding of what osteoarthritis is and on risk factors that predispose to disease occurrence. It concludes with a discussion of the impact of osteoarthritis on disability.
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PMID:Osteoarthritis: new insights. Part 1: the disease and its risk factors. 1103 93

Osteoarthritis is the most common form of arthritis, affecting millions of people in the United States. It is a complex disease whose etiology bridges biomechanics and biochemistry. Evidence is growing for the role of systemic factors, such as genetics, diet, estrogen use, and bone density, and local biomechanical factors, such as muscle weakness, obesity, and joint laxity. These risk factors are particularly important in the weight-bearing joints, and modifying them may help prevent osteoarthritis-related pain and disability. Major advances in management to reduce pain and disability are yielding a panoply of available treatments ranging from nutriceuticals to chondrocyte transplantation, new oral anti-inflammatory medications, and health education. This article is part 2 of a two-part summary of a National Institutes of Health conference that brought together experts in osteoarthritis from diverse backgrounds and provided a multidisciplinary and comprehensive summary of recent advances in the prevention of osteoarthritis onset, progression, and disability. Part 2 focuses on treatment approaches; evidence for the efficacy of commonly used oral therapies is reviewed and information on alternative therapies, including nutriceuticals and acupuncture, is presented. Biomechanical interventions, such as exercise and bracing, and behavioral interventions directed toward enhancing self-management are reviewed. Current surgical approaches are described and probable future biotechnology-oriented approaches to treatment are suggested.
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PMID:Osteoarthritis: new insights. Part 2: treatment approaches. 1177 71

Necrotizing cellulitis and fasciitis may be difficult to recognize. When skin necrosis is not obvious, the diagnosis must be suspected if there are signs of severe sepsis (accelerated heart or respiratory rates, oliguria, mental confusion.) and/or some of the following local symptoms or signs: severe spontaneous pain, indurated edema, bullae, cyanosis, skin pallor, absence of lymphangitis, skin hypoesthesia, crepitation, muscle weakness, foul smell of exudates. Many risk factors are suspected. A recent case-control study demonstrated that using ibuprofen increased the risk of cellulitis complicating chickenpox in children. Evidence is lower for other risk factors that are present with a high prevalence in most series: local lesion of skin or mucous membranes (acute or chronic disease, traumatism, surgery.), diabetes, arteriopathy, alcoholism, obesity, immunosuppression, NSAIDs. The risk of streptococcal necrotizing fasciitis is increased when in contact with patients infected by the same streptococcus.
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PMID:[Necrotizing fasciitis. Clinical criteria and risk factors]. 1131 68

In 2,000 consecutive stroke patients collected in a prospective hospital-based stroke registry over a 10-year period, we assessed whether stroke in men and women was different in respect to vascular risk factors, clinical features and natural history. The frequency of the different variable in men and women was analyzed by means of univariate analysis and logistic regression models. Women accounted for 48% of the study population (n = 967) and were older than men (mean age 75 vs. 69 years, p < 0.001). In the age group of 85 years or older, stroke was more frequent in women than in men (69.8 vs. 30.2%, p < 0.001). Women showed a higher frequency of cardioembolic infarction and a lower occurrence of lacunar infarction and stroke of undetermined cause than men. In-hospital mortality (17.4 vs. 13.3%) and length of hospital stay (19.6 vs. 16.7 days) was significantly higher (p < 0.001) in women than in men. In the model based on demographic variables and cardiovascular risk factors, obesity, heart failure, atrial fibrillation and age were significant predictors of stroke in women, while intermittent claudication, ischemic heart disease, chronic obstructive pulmonary disease, cigarette smoking and alcohol abuse were predictors in male sex. Hypertension and limb weakness were predictors for stroke in women, and absence of neurological deficit at hospital discharge, lacunar syndrome and ataxia were predictors in men in the models based on all variables. Women differ from men in the distribution of risk factors and stroke subtype, stroke severity and outcome. Differences in stroke pathology and/or differences in functional anatomy or plasticity of the brain between sexes may account for these findings.
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PMID:Acute cerebrovascular disease in women. 1138 56

Rheumatoid arthritis is a debilitating, chronic, systemic, autoimmune disease of unknown etiology that causes destruction of joint cartilage and bone. It generally occurs between the fourth and sixth decades of life, and affects two to three times more women than men. It is characterized by joint stiffness, pain, and swelling, and is accompanied by a loss of body cell mass. This loss of cell mass, known as rheumatoid cachexia, predominates in skeletal muscle, but also occurs in the viscera and immune system. Thus, rheumatoid cachexia leads to muscle weakness and a loss of functional capacity, and is believed to accelerate morbidity and mortality in rheumatoid arthritis. Currently there is no established mechanism for rheumatoid cachexia, but it is accompanied by elevated resting energy expenditure, accelerated whole-body protein catabolism, and excess production of the inflammatory cytokines, tumor necrosis factor-alpha and interleukin-1beta. Tumor necrosis factor-alpha is probably the central mediator of muscle wasting in rheumatoid arthritis, and is known to act synergistically with interleukin-1beta to promote cachexia. In general, tumor necrosis factor-alpha and interleukin-1beta are thought to alter the balance between protein degradation and protein synthesis in rheumatoid arthritis to cause muscle wasting. The precise mechanism by which they do this is not known. Reduced peripheral insulin action and low habitual physical activity are important consequences of rheumatoid arthritis, and have also been implicated as mediators of rheumatoid cachexia. Insulin inhibits muscle protein degradation. Consequently, reduced peripheral insulin action in rheumatoid arthritis is thought to be permissive to cytokine-driven muscle loss. The cause of reduced peripheral insulin action in rheumatoid arthritis is not known, but tumor necrosis factor-alpha has been shown to interfere with insulin receptor signaling and is probably an important contributor. Low habitual physical activity has consistently been observed in rheumatoid arthritis and is an important consequence of, and contributor to, muscle wasting. In addition, low physical activity predisposes to fat gain and is believed to precipitate a negative reinforcing cycle of muscle loss, reduced physical function, and fat gain in rheumatoid arthritis, which leads to 'cachectic obesity'. To date, there is no standard treatment for rheumatoid cachexia. However, physical exercise is currently believed to be the most important and clinically relevant countermeasure against rheumatoid cachexia. In general, a combination of skeletal muscle strength training and aerobic exercise is recommended, but must be prescribed with the patient's disease status, overall health, and safety in mind. Future studies should investigate the safety, efficacy, and required dose of anti-cytokine therapy for the treatment of rheumatoid cachexia. In this review, we outline the current definition of rheumatoid cachexia, and discuss the etiology, pathogenesis, and treatment of rheumatoid cachexia.
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PMID:Cachexia in rheumatoid arthritis. 1216 13

The diagnosis of Cushing's syndrome rests on the demonstration of clinical features and biochemical abnormalities that reflect hypercortisolism. If a patient presents with typical clinical features such as weight gain with truncal obesity and supraclavicular fat deposition, wide purple striae, and proximal muscle weakness, the diagnosis is clear-cut and is nearly always substantiated by a 24-hour urine free cortisol excretion value more than four times the normal level. However, many patients present with signs and symptoms that are common in the general population, such as hypertension, generalized weight gain, reproductive abnormalities, and depression. Many of these patients have normal cortisol excretion and do not have Cushing's syndrome. Others have mild hypercortisolism caused by psychiatric disorders, obligate exercise, morbid obesity, sleep apnea, or uncontrolled diabetes mellitus. These patients may be confused with those with the true Cushing's syndrome, and thus are considered to have a "pseudo-Cushing" state. Additional observation over time, and testing with midnight cortisol measurements, the 2-day-2-mg dexamethasone suppression test, or the dexamethasone suppression-CRH stimulation test may be useful to identify true Cushing's syndrome in these patients.
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PMID:Diagnostic tests for Cushing's syndrome. 1238 46

A weakness of many animal models of diabetes mellitus is the failure to use insulin therapy, which typically results in severe body wasting. Data collected from such studies must be interpreted cautiously to separate the effects of hyperglycemia from those of starvation. We provide several algorithms that were used by us in two long-term (20-week) experiments in which hyperglycemia (300 to 400 mg/dl), dyslipidemia (cholesterol [280 to 405 mg/dl] and triglycerides [55 to 106 mg/dl] concentrations), and positive energy balance were maintained in swine. Yucatan miniature swine groups included control, alloxan-induced diabetes mellitus, diabetes mellitus plus diet-induced dyslipidemia, and exercise-trained diabetic dyslipidemic pigs. The algorithms were developed for the porcine model because of several similarities to humans, including: cardiac anatomy and physiology, propensity for sedentary behavior, and metabolism of dietary carbohydrates and lipids. Acute toxic effects of alloxan (hypoglycemia, hyperglycemia, nephrotoxicosis) were minimized by preventive fluid loading and by use of algorithms in which insulin, food, and fluid therapy were administered. Long-term insulin and food maintenance algorithms elicited normal body weight gain in all three diabetic groups (lean experiment) and threefold greater body weight gain in pigs of an obesity experiment. Exercise-trained pigs of both experiments manifested significantly increased work performance and did not experience medical complications. We conclude that these algorithms can be used in swine, or similar algorithms can be developed for other animal species to maintain hyperglycemia and/or dyslipidemia, while avoiding diabetes-induced wasting. Importantly, animal models of diabetes mellitus that maintain positive energy balance and poor glycemic control provide a marked improvement over other models by more closely mimicking the human presentation of diabetes mellitus.
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PMID:Porcine model of diabetic dyslipidemia: insulin and feed algorithms for mimicking diabetes mellitus in humans. 1262 6


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